Chloroform and bromoform were more hepatotoxic than their corresponding deuterated forms, CDC13 and CDBr3. These findings demonstrated that the metabolism of the C-H bond of these haloforms is the rate determining step in their mechanism of bioactivation. In contrast, there was no observable difference in the hepatotoxicity produced by iodoform (CHI3) or halothane (CF3CHBrC1) and their corresponding deuterium labeled derivatives. It thus appears that another biotransformation pathway is the rate determining step in the bioactivation of these compounds into hepatotoxins. The methodology outlined in this report can be applied to studies of the mechanisms of toxicity produced by other halocarbons.